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Acute left ventricular failure - interstitial and alveolar pulmonary edema. Non-cardiogenic pulmonary edema.

Cardiogenic and non-cardiogenic pulmonary edema are considered as the immediate cause of death in every fourth person who died.

Pathogenesis. In a healthy person, the hydrostatic pressure in the pulmonary capillaries is 7–9 mm Hg. Art., it slightly exceeds that in interstitium. The liquid is retained in the capillaries due to its viscous properties, sufficiently high figures of oncotic pressure. Alveolar-but-capillary membranes are semipermeable; minimal fluid flow from the pulmonary capillaries to the interstitium does not lead to pulmonary edema, since excess fluid immediately flows through the lymphatic vessels.

The following factors are necessary for the occurrence of pulmonary edema:

• High hydrostatic pressure (more than 20-30 mm Hg) in the capillaries of the lungs. Such a hemodynamic situation is possible in acute left ventricular failure (myocardial infarction, post-infarction scars, tachyarrhythmias, etc.), mitral stenosis, large transfusions (transfusion of large amounts of fluids in resuscitation, surgical practice, in pregnant women).

• Low, less than 15 mmHg. Art., oncotic plasma pressure. This more rare cause of pulmonary edema is caused by hypoproteinemia after blood loss, with alimentary dystrophy, and liver-cell failure.

• High permeability of the alveolar-capillary membranes in case of infectious-toxic, anaphylactic, enzymatic (pancreatic) shock, chemical and thermal lung trauma, “neurogenic” pulmonary edema in case of strokes, severe traumatic brain injury.

• Negative (less than 20 mm RT. Art.) Intra-alveolar pressure in severe obstruction of the upper respiratory tract in patients with sublingual laryngitis, asphyxia of foreign bodies of the trachea;

with drowning; overly active ventilation regimen.

When pulmonary edema occurs, a self-sustaining thanatogenic vicious circle begins to “work”:

The variety of causes of pulmonary edema allows us to consider it a typical pathological process. Modern science has not answered A. Sop-heim's question: is pulmonary edema a cause of death, or does pulmonary edema arise because the patient has come to die (ie, the patient “dies through the mechanism of pulmonary edema”).

Cardiogenic pulmonary edema

Acute left jelly ud spectacle failure - cardiogenic interstitial and alveolar pulmonary edema - occurs with myocardial infarction, post-infarction cardiosclerosis, cardiomyopathies, acquired and congenital heart defects. The likelihood of acute left ventricular failure increases dramatically with max and systolic paroxysmal arrhythmias, hypertensive crises.

The left ventricle loses the ability to "pump" all the blood entering it during diastole, hence the increase in the final diastolic pressure in the left ventricle, hydrostatic pressure in the pulmonary veins, then in the capillaries and arteries. Due to the sharp increase in hydrostatic pressure in the pulmonary capillaries, the fluid extravasation in the interstitium increases, and the resorptive mechanisms become insolvent. Interstitial pulmonary edema develops into alveolar. If the vicious circle of pulmonary edema (see above) cannot be broken, a lethal outcome occurs.

Clinic, diagnostics. Interstitial pulmonary edema has the clinical equivalent of paroxysm of mixed dyspnea ("cardiac asthma"). The patient's position is forced, half-sitting. Acrocyanosis. Tachypnea, tachycardia. In the lungs, breathing is weak or hard, scattered dry rales. In patients with chronic heart failure under the shoulder blades, sonorous, finely bubbly, moist rales can be heard.

Alveolar pulmonary edema is characterized by the addition of moist rales to the described symptoms, starting from the roots of the lungs (interscapular spaces), then along all pulmonary fields. Breathing becomes bubbling, sometimes heard from a distance. With cough, foamy whitish-pink sputum is secreted. With auscultation of the heart - gag-like rhythms. Tachycardia.

Radiologically, with interstitial edema, the pulmonary pattern appears fuzzy, "smeared." In the basal sections, a decrease in transparency, the expansion of interlobar partitions. In the basal-lateral sections and basal zones of the Curly line, peribronchial and perivascular shadows due to the accumulation of transudate in the interstitial tissue.

Alveolar pulmonary edema from the perspective of the X-ray method has several forms: central (with symmetric homogeneous darkening of high intensity in the central sections of the pulmonary fields); diffuse (with shadows of different intensities); focal (with limited or confluent round-shaped blackouts, capturing several segments or lung lobes).

The course of pulmonary edema can be acute (up to 4 hours) with myocardial infarction, mitral stenosis, anaphylactic shock, cerebral stroke; subacute (4-12 hours) - with myocardial infarction, acquired and congenital heart defects, pneumonia; protracted (over 12 hours) - in patients with myocardial diseases, post-infarction cardiosclerosis, atrial fibrillation.

In the structure of the clinical diagnosis, cardiogenic and non-cardiogenic pulmonary edema is always listed under “complications of the underlying disease”.

• coronary heart disease; Transmural anterior septal myocardial infarction (date, hour).

Complication. Cardiogenic alveolar pulmonary edema, acute course (date, hour).

• Rheumatism, inactive phase. Combined mitral defect with a predominance of stenosis of the left atrioventricular opening. Atrial fibrillation, tachysystolic form.
Chronic heart failure 3 f. class (H 2 A).

Complication. Interstitial pulmonary edema, prolonged course (date, hour).

Urgent care.

Universal methods of life support:

- reassure the patient;

- if the blood pressure is elevated or normal, give the patient a semi-sitting position;

- inhalation of moistened oxygen through the nasal cannula. The mask is less acceptable because in a state of suffocation, it is poorly tolerated;

- defoamers: inhalation of a 30% aqueous solution of ethyl alcohol or 2-3 ml of a 10% alcohol solution of antifomsilan. In severe cases, endotracheal administration of 2-4 ml of a 96% solution of ethyl alcohol;

- increase in breathing resistance - exhale through a tube lowered into a jar of water;

- elimination of hypercatecholaminemia by the introduction of droperidol or relanium, or narcotic analgesics into a vein.

Differentiated events:

• In case of toxic pulmonary edema (inhalation of phosgene, ozone, nitric oxide, cadmium oxide, monochloromethane, etc.; endotoxicosis with sepsis, peritonitis, meningococcal and non-clostridial anaerobic infections, pancreatitis, hantavirus pulmonary syndrome, severe allergies, inhalation and smoke inhalation, toxicosis ) at the prehospital stage, prednisone is injected into the vein with a bolus of 90-120 mg, up to 1.2-2 g / day. In case of inhalation lesions - becotide or another inhaled glucocorticosteroid 4 breaths every 10 minutes until the inhaler is completely emptied, calculated for 200-250 doses (V. Alekseev, V. Yakovlev, 1996).

To create an excess gradient in order to direct the fluid flow from interstitium into the vascular bed, it is necessary to increase the oncotic pressure of the plasma. A 10-20% albumin solution up to 200-400 ml / day is injected into a vein. Immediate call resuscitation ambulance team. Intubation, mechanical ventilation allow even patients with hantavirus pulmonary syndrome to be saved (O.A. Alekseev, V.I. Roshchupkin, 1997).

• With cardiogenic pulmonary edema, events are determined by blood pressure (BP) figures.

- If blood pressure is elevated, nitroglycerin is given sublingually repeatedly, clonidine 0.25% 1-1.5 ml is administered intravenously in an isotonic solution, lasix in a dose of 40-80 mg, if necessary, again morphine or relanium. In severe cases, sodium nitroprusside 30 mg or nitroglycerin 5-10 mg intravenously. Sodium nitroprusside (napiprus, niprid) 30 mg in 400 ml of glucose begin to be administered at a rate of 6 cap./min with a gradual increase. Mandatory constant monitoring of blood pressure, which should not be reduced to numbers below 90/60 mm RT. Art.! Side effects can be (except hypotension) vomiting, abdominal pain, arrhythmias. The most convenient form of nitroglycerin for drip into a vein is perlinganite - ampoules containing 10 ml of a 0.1% solution of nitroglycerin in glucose (1 mg in 1 ml). A 0.01% solution is introduced at an initial rate of 25 μg / min, which corresponds to 1 ml of a 0.01% solution in 4 minutes. Mandatory constant monitoring of blood pressure!

- With normal blood pressure: nitroglycerin sublingually repeatedly, lasix intramuscularly or intravenously at a dose of 40-80 mg, relanium or morphine into a vein. In severe cases, nitroglycerin is administered intravenously.

- The most difficult clinical situation is pulmonary edema with low blood pressure. The patient’s supine position. Dopamine intravenously: ampoules containing 5 ml of a 0.5% solution (25 mg of dry matter) or 5 ml of a 4% solution (200 mg of dry substance) are used. 200 mg of dopamine is added to 400 ml of 5% glucose, the initial rate of administration is 2-10 drops / min.

An alternative is the administration of dobutamine. Dobutamine is available in 20 ml vials and 5 ml ampoules containing 250 mg of dry matter. The contents of the vial or ampoule are diluted in 400 ml of 5% glucose. The introduction is drip, the initial rate of administration is 5-10 drops / min. If long-term administration of dobutamine or dopamine is required, norepinephrine is additionally administered (per 400 ml of liquid 1 ml of a 0.1% solution of the drug).

If it is possible to increase blood pressure, lasix and nitroglycerin are administered.

Specific clinical situations

• In case of myocardial infarction, good analgesia is necessary (fentanyl 0.005% 1-2 ml jet in a vein in combination with 2-4 ml 0.25% droperidol solution). If the numbers allow blood pressure, an isoket is injected dropwise into a vein (each ampoule contains 10 mg of dry matter in 10 ml of isotonic sodium chloride solution). The contents of 5 ampoules are added to 500 ml of the infused solution, the drug is administered dropwise into a vein, the initial speed is 3-7 drops / min, followed by a gradual increase. Mandatory constant monitoring of blood pressure!

• In case of paroxysmal tachyarrhythmia - universal antiarrhythmic drugs (ethmosin, etacisin, cordarone, novocainamide, in case of ventricular tachycardia - 10-15 ml of 1% lidocaine solution, 20 ml of panangin in a vein, 4 units of simple insulin per 250 ml of 5% glucose). With the ineffectiveness of a single injection into the vein of an antiarrhythmic drug - electrical depolarization of the heart!

• With mitral stenosis, the method of choice is the intravenous administration of morphine or its analogues, with normal or high blood pressure - 0.3-0.5-1 ml of pentamine or benzohexonium, depending on the numbers of blood pressure. At low blood pressure, it is advisable to inject 30-90 mg of prednisolone into a vein.

Criteria for the transportability of a patient who has experienced pulmonary edema: the disappearance of foamy sputum, moist rales over all pulmonary fields, the absence of a repeated attack of suffocation in the horizontal position of the patient, stabilization of the number of breaths 22-26 in 1 min. During transportation, oxygen inhalation.
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Acute left ventricular failure - interstitial and alveolar pulmonary edema. Non-cardiogenic pulmonary edema.

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